Oct. 13, 2004 -- After years of searching, scientists may have solved one of the biggest mysteries of hearing.
The discovery centers on a protein called TRPA1, which is found on the tips of specialized sensory cells in the inner ear.
TRPA1 may be responsible for turning sounds into nerve impulses that the brain can interpret, according to a study in the Oct. 13 advanced online edition of the journal Nature.
The finding comes from researchers at several institutions. Experts collaborated from Harvard Medical School, Boston's Dana-Farber Cancer Institute, Northwestern University Institute for Neurosciences, the University of Virginia School of Medicine, Massachusetts Institute of Technology, Harvard-Partners Genome Center, Duke University Medical Center, and the National Institutes of Health.
"People have been looking for this protein for a decade," says researcher David Corey, a Harvard neurobiology professor, in a news release.
Hearing Protein Found
TRPA1's role in hearing was identified through a series of experiments with mice and zebrafish.
Here's how this "hearing" protein works, according to a news release.
The TRPA1 molecule forms an inactive channel in tiny hair cells located deep within the inner ear, the structure, which control hearing and balance. The channel is shaped like a donut and when activated the donut "hole" pops open. Activation of the channel occurs when sound strikes structure creating an electrical signal, which is sent to the brain.
Scientists have long thought that that was probably how hearing reached the brain, but they couldn't identify the key protein before now.
"This opens a window of opportunity with significant implications for the field of hearing and deafness research and beyond, including the fields of engineering and nanotechnology," says University of Virginia researcher Gwenäelle Géléoc, assistant professor of research in neuroscience and otolaryngology, in a news release.
For instance, the finding could lead to new gene therapies for deafness and balance problems, since people with those conditions may have a mutated form of the gene that makes TRPA1.
Such developments on hearing could come "in the next five to 10 years," says Jeffrey Holt, University of Virginia assistant professor of neuroscience and otolaryngology (and Géléoc's husband), in a news release.
"Essentially, if we could take a correct copy of the gene and reintroduce it into the cells of the inner ear, we might be able to restore hearing and balance function in people with hereditary inner ear disorders," says Holt.